DMBA/TPA-induced tumor formation is aggravated in human papillomavirus type 16 E6/E7 transgenic mouse skin

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dc.contributor.authorM O Kim-
dc.contributor.authorS H Kim-
dc.contributor.authorM J Shin-
dc.contributor.authorD H Yu-
dc.contributor.authorB S Kim-
dc.contributor.authorKyu Tae Chang-
dc.contributor.authorS Lee-
dc.contributor.authorY B Park-
dc.contributor.authorT H Lee-
dc.contributor.authorZ Y Ryoo-
dc.date.accessioned2017-04-19T09:07:26Z-
dc.date.available2017-04-19T09:07:26Z-
dc.date.issued2007-
dc.identifier.issn09650407-
dc.identifier.uri10.3727/000000006783980964ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/7948-
dc.description.abstractHuman papillomavirus type 16 (HPV16) is a major causative factor in the development of uterine cervical carcinomas. We investigated the role of E6/E7 in tumor formation. Skin-specific E6/E7 transgenic mice showed approximately twice as many tumors compared with nontransgenic mice in dimethylbenz[a]anthracene (DMBA)-initiated and a 12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted two-stage skin carcinogenesis. This model showed a significant increase of epidermal cell proliferation in the transgenic mice. The 8-hydroxy- 2'deoxyguanosine (8OH-dG) detection assay showed that oxidative DNA damage was significantly higher in the transgenic mice after TPA treatments. The overexpression of E6/E7 in the skin in the DMBA/TPA two-stage-induced carcinogenesis model aggravated the incidence of tumor formation. HPV16 E6/E7 appears to act as an enhancer of carcinogenesis that requires initiation by DMBA and promotion by TPA.-
dc.publisherCognizant Communication Corp-
dc.titleDMBA/TPA-induced tumor formation is aggravated in human papillomavirus type 16 E6/E7 transgenic mouse skin-
dc.title.alternativeDMBA/TPA-induced tumor formation is aggravated in human papillomavirus type 16 E6/E7 transgenic mouse skin-
dc.typeArticle-
dc.citation.titleOncology Research-
dc.citation.number7-
dc.citation.endPage332-
dc.citation.startPage325-
dc.citation.volume16-
dc.contributor.alternativeName김명옥-
dc.contributor.alternativeName김성현-
dc.contributor.alternativeName신미정-
dc.contributor.alternativeName유동훈-
dc.contributor.alternativeName김봉수-
dc.contributor.alternativeName장규태-
dc.contributor.alternativeName이상규-
dc.contributor.alternativeName박용복-
dc.contributor.alternativeName이태훈-
dc.contributor.alternativeName류 재영-
dc.identifier.bibliographicCitationOncology Research, vol. 16, no. 7, pp. 325-332-
dc.identifier.doi10.3727/000000006783980964-
dc.subject.keywordDMBA/TPA-
dc.subject.keywordhK14 promoter-
dc.subject.keywordHPV16 E6/E7-
dc.subject.keywordKeratinocytes-
dc.subject.keywordSkin cancer-
dc.subject.keywordTransgenic mice-
dc.subject.localDMBA/TPA-
dc.subject.localhK14 promoter-
dc.subject.localHPV16 E6/E7-
dc.subject.localKeratinocytes-
dc.subject.localKeratinocyte-
dc.subject.localSkin cancer-
dc.subject.localTransgenic mice-
dc.subject.localTransgenic mouse-
dc.description.journalClassY-
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